Die Attraktivität von Handelsmarken-Käufern : eine empirische Analyse und strategische Empfehlungen zur Vermarktung von Handelsmarken

Im internationalen Vergleich ist der Marktanteil von Handelsmarken (bzw. Eigenmarken) im deutschen Lebensmitteleinzelhandel extrem hoch. Dies wird zwar stark durch den Erfolg des Discounters Aldi beeinflusst, doch auch im übrigen Einzelhandel weisen Handelsmarken zum Teil ein beträchtliches Wachstum auf. Dieser Trend wird sich aller Erwartung nach fortsetzen. Als Motiv des Handelmarkeneinsatzes wird häufig - neben dem Preiskampf gegen Discounter - die Profilierung der eigenen Geschäftsstelle genannt, die zur Stärkung der Kundenbindung führen soll. Aber sind Handelsmarkenkäufer tatsächlich geschäftstreuer? Dies ist eine von vielen Fragen, denen in der vorliegenden Studie nachgegangen wird. In dieser Untersuchung wird der deutsche Handelsmarkenkäufer anhand marketing-relevanter Merkmale analysiert. So lässt sich ein Eindruck gewinnen, ob Handelsmarkenkäufer aufgrund ihrer spezifischen Charakteristika ein attraktives Kundensegment darstellen. Hierzu werden Verbraucher auf Grundlage von Kassenzetteldaten - ergänzt durch eine schriftliche Befragung - zunächst in drei Gruppen mit unterschiedlicher Handelsmarken-Kaufintensität eingeteilt und anschießend mit einander verglichen. Die analysierten Größen umfassen u.a. die Qualitätsbeurteilung von Handelsmarken, die Treue gegenüber Marken und Einkaufsstätten, die Bedeutung von Preis und Qualität bei der Kaufentscheidung sowie die soziodemographischen Merkmale Alter, Geschlecht, Familiengröße, Bildung und Einkommen. Im Ergebnis kann ein sehr präzises und stimmiges Bild des deutschen Handelsmarkenkäufers gezeichnet werden. Hieraus werden strategische Empfehlungen zum Umgang mit Handelsmarken abgeleitet

Successful radiation treatment of anaplastic thyroid carcinoma metastatic to the right cardiac atrium and ventricle in a pacemaker-dependent patient

Anaplastic thyroid carcinoma (ATC) is a rare, aggressive malignancy, which is known to metastasize to the heart. We report a case of a patient with ATC with metastatic involvement of the pacemaker leads within the right atrium and right ventricle. The patient survived external beam radiation treatment to his heart, with a radiographic response to treatment. Cardiac metastases are usually reported on autopsy; to our knowledge, this is the first report of the successful treatment of cardiac metastases encasing the leads of a pacemaker, and of cardiac metastases from ATCs, with a review of the pertinent literature

Chronic sleep restriction induces long-lasting changes in adenosine and noradrenaline receptor density in the rat brain

Although chronic sleep restriction frequently produces long-lasting behavioural and physiological impairments in humans, the underlying neural mechanisms are unknown. Here we used a rat model of chronic sleep restriction to investigate the role of brain adenosine and noradrenaline systems, known to regulate sleep and wakefulness, respectively. The density of adenosine A1 and A2a receptors and β-adrenergic receptors before, during and following 5 days of sleep restriction was assessed with autoradiography. Rats (n = 48) were sleep-deprived for 18 h day(-1) for 5 consecutive days (SR1-SR5), followed by 3 unrestricted recovery sleep days (R1-R3). Brains were collected at the beginning of the light period, which was immediately after the end of sleep deprivation on sleep restriction days. Chronic sleep restriction increased adenosine A1 receptor density significantly in nine of the 13 brain areas analysed with elevations also observed on R3 (+18 to +32%). In contrast, chronic sleep restriction reduced adenosine A2a receptor density significantly in one of the three brain areas analysed (olfactory tubercle which declined 26-31% from SR1 to R1). A decrease in β-adrenergic receptors density was seen in substantia innominata and ventral pallidum which remained reduced on R3, but no changes were found in the anterior cingulate cortex. These data suggest that chronic sleep restriction can induce long-term changes in the brain adenosine and noradrenaline receptors, which may underlie the long-lasting neurocognitive impairments observed in chronic sleep restriction

MTO1-deficient mouse model mirrors the human phenotype showing complex I defect and cardiomyopathy

Recently, mutations in the mitochondrial translation optimization factor 1 gene (MTO1) were identified as causative in children with hypertrophic cardiomyopathy, lactic acidosis and respiratory chain defect. Here, we describe an MTO1-deficient mouse model generated by gene trap mutagenesis that mirrors the human phenotype remarkably well. As in patients, the most prominent signs and symptoms were cardiovascular and included bradycardia and cardiomyopathy. In addition, the mutant mice showed a marked worsening of arrhythmias during induction and reversal of anaesthesia. The detailed morphological and biochemical workup of murine hearts indicated that the myocardial damage was due to complex I deficiency and mitochondrial dysfunction. In contrast, neurological examination was largely normal in Mto1-deficient mice. A translational consequence of this mouse model may be to caution against anaesthesia-related cardiac arrhythmias which may be fatal in patients

Generation of <i>Mto1</i> knockdown mice by gene trap mutagenesis.

<p>(A) Integration of gene trap vector U3CEO in intron 6 of <i>Mto1</i>. Arrows indicate amplificons for RT-PCR. (B) RT-PCR of heart tissue shows reduced levels of <i>Mto1</i> transcripts using primers covering sequences 5′ or 3′ to the integration site, ***p<0.001. (C) Western blot showing a clear reduction of MTO1 protein in <i>Mto1</i>−/− mouse embryonic fibroblasts as compared to <i>Mto1</i>+/+ controls.</p

Heart weight related to body weight was significantly increased in <i>Mto1</i>−/− mutant mice as compared to controls, both in 5 months old mice (n = 15, *p<0.05) and as a trend in 10 months old mice (n = 8, n.s.).

<p>Heart weight related to body weight was significantly increased in <i>Mto1</i>−/− mutant mice as compared to controls, both in 5 months old mice (n = 15, *p<0.05) and as a trend in 10 months old mice (n = 8, n.s.).</p

Behavioral analysis of <i>Mto1</i> mutant mice using a modified holeboard.

<p><i>Mto1</i>−/−mice show increased horizontal locomotor activity (A) as well as increased mean velocity (B) as compared to controls. Anxiety-related behavior measured via the time on board (C) and group contact (D) was also significantly changed; object exploration was increased (E) and acoustic startle response decreased (F), *p<0.05; **p<0.01.</p